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Oat β-glucan inhibits adipogenesis and hepatic steatosis in high fat diet-induced hyperlipidemic mice via AMPK signaling
Journal of Functional Foods ( IF 5.6 ) Pub Date : 2017-12-22 , DOI: 10.1016/j.jff.2017.12.045
Bo Liu , Tao Yang , Yi Luo , Linna Zeng , Limin Shi , Chengxi Wei , Ying Nie , Yu Cheng , Qinlu Lin , Feijun Luo

To evaluate the lowering-lipid effect of oat β-glucan (OβG) and its molecular mechanism, high-fat diet (HFD)-induced hyperlipidemic mouse model and oleic acid-induced lipid accumulation model of HepG2 cells were used in this study. OβG obviously reduced HFD-induced the gain of body weight and epididymal fat pad, and inhibited hepatic adipocyte hyperplasia. These effects were associated with the down-regulation of FAS and SREBP-1, up-regulation of PPARα and particularly the activation of AMP-activated protein kinase (AMPK) signaling in both liver and fat tissues. In the oleic acid-induced HepG2 cells, OβG partly suppressed lipogenesis and activated AMPK. OβG inhibited lipid metabolism-related protein expressions such as FAS, SREBP-1, CPT-1, PPARα and activating ACC, which are the downstream targets of AMPK. Taken together, our results suggest that administration of OβG exerts lipid-lowering effect in HFD mice via AMPK signal pathway, which provide novel application for the prevention and treatment of hyperlipidemia.



中文翻译:

燕麦β-葡聚糖通过AMPK信号传导抑制高脂饮食诱导的高脂血症小鼠的脂肪形成和肝脂肪变性

为了评估燕麦β-葡聚糖(OβG)的降血脂作用及其分子机制,本研究使用高脂饮食(HFD)诱导的高脂血症小鼠模型和油酸诱导的HepG2细胞脂质蓄积模型。OβG明显降低了HFD诱导的体重增加和附睾脂肪垫,并抑制了肝脂肪细胞的增生。这些作用与肝和脂肪组织中FAS和SREBP-1的下调,PPARα的上调,特别是AMP激活的蛋白激酶(AMPK)信号的激活有关。在油酸诱导的HepG2细胞中,OβG部分抑制脂肪生成并激活AMPK。OβG抑制了脂质代谢相关蛋白的表达,例如FAS,SREBP-1,CPT-1,PPARα和激活性ACC,它们是AMPK的下游靶标。在一起

更新日期:2017-12-22
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